Evidence map›Paper›PMID 1314162›Full record

ArticleThe EMBO journal1992

Dissection of the interferon gamma-MHC class II signal transduction pathway reveals that type I and type II interferon systems share common signalling component(s).

J E Loh, C H Chang, W L Fodor, R A Flavell

Abstract read
In one paragraph

Article in The EMBO journal, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed.

  1. Trial
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  6. Review
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  16. Mutant human cells defective in induction of major histocompatibility complex class II genes by interferon gamma.Proceedings of the National Academy of Sciences of the United States of America · 1993
    Article
  17. Article
  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

J E LohHoward Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06510.
C H Chang
W L Fodor
R A Flavell

Funding

A retrievable autologous bioengineered esophageal implant as a novel treatment for long-gap esophageal atresiaR44HD095784 · NICHD · BIOSTAGE, INC. · PI FINCK, CHRISTINE M, FODOR, WILLIAM L · 2018 to 2020
$1.8M
NICHD NIH HHS R44 HD095784
6 · The paper itself

Abstract

We have used a herpes virus thymidine kinase (HSV-TK) based metabolic selection system to isolate mutants defective in the interferon gamma mediated induction of the MHC class II promoter. All the mutations act in trans and result in no detectable induction of MHC and invariant chain (Ii) gene expression. Scatchard analysis indicates that the mutants have a normal number of surface IFN gamma receptors with the same affinity constant. The mutants fall into two broad categories. One class of mutants is still able to induce MHC class I, IRF-1, 9-27, 1-8 and GBP genes by IFN gamma. A second class of mutants is defective for the IFN gamma induction of all the genes tested; surprisingly, the IFN alpha/beta induction of MHC class I, 9-27, ISG54 and ISG15 genes is also defective in these mutants, although different members of this class can be discriminated by the response of the GBP and IRF-1 genes to type I interferons. These data demonstrate that the signalling pathways of both type I and type II interferon systems share common signal transduction component(s). These mutants will be useful for the study of IFN gamma regulation of class II genes and Ii chain, and to elucidate molecular components of type I and type II interferon signal transduction.

Indexed as

Genes, MHC Class IIMutagenesisBase SequenceDNA ProbesEthyl MethanesulfonateGenes, ViralHeLa CellsHLA-D AntigensHumansInterferon-gammaInterferon Type IMajor Histocompatibility ComplexMolecular Sequence DataOligodeoxyribonucleotidesPlasmidsPromoter Regions, GeneticDNA ProbesEthyl MethanesulfonateHLA-D AntigensInterferon-gammaInterferon Type IOligodeoxyribonucleotidesThymidine KinaseViral Structural Proteins

Identifiers

PMID1314162
PMCPMC556584

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.